Juçara pulp supplementation improves glucose tolerance in mice.

BACKGROUND: The consumption of hyperlipidic and hypercaloric diet is considered a major factor to promote obesity and the consumption of food with antioxidant properties, like Juçara (Euterpe edulis Mart), could be a tool to prevent the deleterious effect of high white adipose deposition. The aim of the present study was to evaluate the effect of administration of juçara pulp in mice fed a high-fat, high-calorie diet on glucose tolerance and adipose tissue inflammatory status. METHODS: Mice were distributed into the following groups: control diet; control diet plus 0.5 % of juçara; control diet plus 2 % of juçara; hypercaloric and hyperlipidic diet; hypercaloric and hyperlipidic diet plus 0.5 % of juçara and hypercaloric and hyperlipidic diet plus 2 % of juçara. Treatments started when mice were 8 weeks old and carried on for a total period of 10 weeks. The serum glucose, triacylglycerol, total cholesterol, insulin, adiponectin, lipopolysaccharides and free fatty acids concentrations were measured. Oral glucose tolerance test was performed. TNF-α, IL-6, and IL-10 protein level were determined by ELISA on mesenteric and epididymal white adipose tissues. Determination of catalase activity was realized in the same tissues. Data were analysed using one-way analysis of variance and post hoc analysis was performed with the Tukey's test. RESULTS: The addition of 0.5 % juçara improved glycemic response in animals that consumed normocaloric as well as hypercaloric and hyperlipidic diets (HC). Supplementation with 0.5 and 2 % did not change the body composition of animals that received the HC diet; however, the animals fed the normocaloric diet with 2 % juçara gained body mass. An intake of 2 % juçara in the HC diet promoted a reduction of catalase activity and IL-10 level in epididymal adipose tissue. CONCLUSIONS: These results suggest that with the administration of 0.5 % juçara, the beneficial effects of polyphenols overcome the deleterious effects of macronutrient composition of juçara, whereas with the administration of 2 % juçara promotes damage by the composition of the fruit and overshadows the beneficial effects of polyphenols on glucose metabolism. On the other hand, higher juçara supplementation improves the inflammatory status targeted by the HC diet.

Reduction in saturated fat intake improves cardiovascular risks in obese adolescents during interdisciplinary therapy.

BACKGROUND/OBJECTIVES: Obesity is related to inflammation and cardiovascular disease. The increase in saturated fatty acid intake (SFA) can potentiate cardiovascular risks. The aim of this study was to assess the influence of change in SFA on carotid intima-media thickness (cIMT), metabolic profile and anti/pro-inflammatory adipokines in obese adolescents. METHODS: Sixty obese adolescents were subjected to 1 year of interdisciplinary intervention (nutrition, psychology, physical exercise and clinical therapy). Blood glucose, insulin, lipid profile, leptin and adiponectin were analysed. Insulin resistance was estimated by HOMA-IR and HOMA-AD. cIMT was measured by ultrasonography. Dietetic intake was calculated by 3-day dietary record. Volunteers were analysed according to tertiles of change (Δ) in SFA intake: Low-SFA reduction<3.68 g; Moderate-SFA reduction 3.68-13.67 g; and High-SFA reduction>13.67 g. RESULTS: Moderate and High-SFA tertiles presented reduction in insulin, leptin/adiponectin ratio, cIMT and increase in adiponectin and adiponectin/leptin ratio. Adiponectin/leptin ratio was predictor of cIMT. HOMA-IR, total cholesterol and LDL-cholesterol reduced only in High-SFA tertile, and was associated with SFA independent of visceral fat. Negative correlations between Δ of SFA and adiponectin and adiponectin/leptin ratio were observed. CONCLUSION: Obese adolescents with moderate and high reduction in SFA presented improvements on pro/anti-inflammatory biomarkers and cIMT, leading to reduction in cardiovascular risks.

Saturated fatty acid intake can influence increase in plasminogen activator inhibitor-1 in obese adolescents.

The aim of this study was to verify if saturated fatty acid intake adjusted by tertiles can influence metabolic, inflammation, and plasminogen activator inhibitor-1 (PAI-1) in obese adolescents. Body mass, height, body mass index, waist circumference, blood pressure, and body composition of 108 obese adolescents were obtained. Fasting glucose, insulin, PAI-1, and CRP were determined. Insulin resistance was assessed by Homeostasis Model Assessment (HOMA-IR) and insulin sensitivity by Quantitative Insulin Sensitivity Check Index (QUICKI). Dietetic intake was estimated by a 3-day dietary record, and volunteers were divided according to consumption of saturated fatty acids: tertile 1 [Low Saturated Fatty Acid Intake (Low-SFA): ≤12.14 g], tertile 2 [Moderate Saturated Fatty Intake (Moderate SFA intake): 12.15-20.48 g], and tertile 3 [High Saturated Fatty Acid Intake (High-SFA Intake); >20.48 g]. Statistical analysis was performed using STATISTICA 7.0 software and the significance level was set at p<0.05. The most important finding in the present study is that Moderate and High-SFA intakes presented significantly higher values of PAI-1 than Low-SFA Intake. PAI-1 was positively associated with saturated fatty intake, waist circumference, mean blood pressure, and HOMA-IR. SFA intake was predictor of PAI-1 independent of body fat, HOMA-IR and total-cholesterol. In addition, PAI-1 was an independent predictor of blood pressure. HOMA-IR and QUICKI presented significantly higher and lower, respectively, in High-SFA compared to Moderate-SFA intake. High-SFA influenced cardiovascular disease risks, since it increased PAI-1 and insulin resistance, and decreased insulin sensibility, leading to vicious cycle among food ingestion, pro-thrombotic state, and cardiovascular risks in obese adolescents.

Chronic exercise promotes alterations in the neuroendocrine profile of elderly people.

Aging and physical inactivity are 2 factors that favour the development of cardiovascular disease, metabolic syndrome, obesity, and diabetes. In contrast, adopting a habitual moderate exercise routine may be a nonpharmacological treatment alternative for neuroendocrine aging disorders. We aimed to assess the effects of moderate exercise training on the metabolic profiles of elderly people with sedentary lifestyles. Fourteen sedentary, healthy, elderly male volunteers participated in a moderate training regimen for 60 min/day, 3 days/week for 24 weeks at a work rate equivalent to their ventilatory aerobic threshold. The environment was maintained at a temperature of 23±2°C, with a humidity of 60±5%. Blood samples for analysis were collected at 3 intervals: at baseline (1 week before training began), and 3 and 6 months after training. The training promoted increased aerobic capacity (relative VO(2), and time and velocity to VO(2)max; (p<0.05)) and reduced serum α-MSH (p<0.05) after 3 months of training when compared with the baseline data. In addition, serum thyroid hormone (T3 and T4) was reduced after 6 months of training compared with baseline levels. Our results demonstrate that a moderate exercise training protocol improves the metabolic profile of older people, and metabolic adaptation is dependent on time.

The role of orexigenic and anorexigenic factors in an interdisciplinary weight loss therapy for obese adolescents with symptoms of eating disorders.

AIM: The aim of this study was to evaluate the role of orexigenic and anorexigenic factors in an interdisciplinary weight loss therapy for obese adolescents with symptoms of eating disorders. METHODS: Thirty-seven post-pubertal, obese adolescents (14 to 19 years old) with symptoms of eating disorders were submitted to long-term interdisciplinary therapy (1 year). Bulimic and binge eating symptoms were measured using the Bulimic Investigatory Test, Edinburgh, and the Binge Eating Scale respectively. Neuropeptide Y, melanin-concentrating hormone, total ghrelin, alpha-melanocyte stimulating hormone and leptin were measured using radioimmunoassay. RESULTS: After long-term interdisciplinary therapy, the adolescents showed significantly improved body composition, visceral and subcutaneous fat and reduced symptoms of bulimia and binge eating. Intriguingly, orexigenic peptides were up-regulated after short-term therapy and down-regulated at the end of therapy, whereas the anorexigenic pathway was improved with therapy. Furthermore, after long-term therapy, a negative correlation was observed between leptin concentration and melanin-concentrating hormone. DISCUSSION: We suggest that long-term therapy promotes an intrinsic association between weight loss, improvement of eating disorder symptoms and a decrease in orexigenic factors. Together, these results represent a more effective course by which patients can normalise behaviours related to eating disorders as well the actions of hormones involved in energy balance, and thus advance obesity control. CONCLUSION: Long-term interdisciplinary therapy was effective to improve anorexigenic and orexigenic factors that influence energy balance and avoid the development of eating disorders in obese adolescents. However, the associations between eating disorders and neuroendocrine factors need to be confirmed in future studies.

Electroacupuncture promotes a decrease in inflammatory response associated with Th1/Th2 cytokines, nitric oxide and leukotriene B4 modulation in experimental asthma.

Previously, we have shown that electroacupuncture (EA) in rats decreased eosinophil infiltration into the pulmonary tissue (PT) and in the bronchoalveolar lavage (BAL) in an experimental model of asthma. Th2 cytokines, leukotriene B4 (LTB4) and nitric oxide (NO) are involved in the asthma inflammatory process. The aim of this study was to verify the effects of EA on these asthma mediators. Male Wistar rats were divided into control (C), immobilized (I), sham acupuncture (SA), and acupuncture (A) groups. All rats were sensitized, and EA treatment using clinical acupuncture points was started 24h after antigen priming. EA was done every other day for 2weeks. Subsequently, animals were challenged by inhalation and sacrificed 24h later. At this time, the BAL and lungs were collected and used to analyze cytokine production, LTB4 and NO. The EA increased IL-1 and IFN-gamma and decreased IL-4, IL-10, NO and LTB4 in the BAL and PT compared to the C and SA groups. The presence of eosinophils in the BAL negatively correlated with IL-1 and IFN-gamma production and positively correlated with IL-4 and IL-10 production. Our results show that the beneficial anti-inflammatory action of EA on asthma is related to the balance of the Thl/Th2 response and the reduction of LTB4 and NO. These results suggest that EA therapy could be an important complementary treatment for asthma.

The effect of thyroid hormones on the white adipose tissue gene expression of PAI-1 and its serum concentration

Metabolic syndrome is associated with an increased risk of developing cardiovascular diseases and Plasminogen activator inhibitor 1 (PAI-1) overexpression may play a significant role in this process. A positive correlation between adipose tissue gene expression of PAI-1 and its serum concentration has been reported. Furthermore, high serum levels of thyroid hormones (T3 and T4) and PAI-1 have been observed in obese children. The present study evaluates the impact of thyroid hormone treatment on white adipose tissue PAI-1 gene expression and its serum concentration. Male Wistar rats (60 days old) were treated for three weeks with T4 (50 µg/day, Hyper) or with saline (control). Additionally, 3T3-L1 adipocytes were treated for 24 h with T4 (100 nM) or T3 (100 nM). PAI-1 gene expression was determined by real-time PCR, while the serum concentration of PAI-1 was measured by ELISA using a commercial kit (Innovative Research, USA). Both the serum concentration of PAI-1 and mRNA levels were similar between groups in retroperitoneal and epididymal white adipose tissue. Using 3T3-L1 adipocytes, in vitro treatment with T4 and T3 increased the gene expression of PAI-1, suggesting non-genomic and genomic effects, respectively. These results demonstrate that thyroid hormones have different effects in vitro and in vivo on PAI-1 gene expression in adipocytes.

The effect of thyroid hormones on the white adipose tissue gene expression of PAI-1 and its serum concentration.

Metabolic syndrome is associated with an increased risk of developing cardiovascular diseases and Plasminogen activator inhibitor 1 (PAI-1) overexpression may play a significant role in this process. A positive correlation between adipose tissue gene expression of PAI-1 and its serum concentration has been reported. Furthermore, high serum levels of thyroid hormones (T3 and T4) and PAI-1 have been observed in obese children. The present study evaluates the impact of thyroid hormone treatment on white adipose tissue PAI-1 gene expression and its serum concentration. Male Wistar rats (60 days old) were treated for three weeks with T4 (50 microg/day, Hyper) or with saline (control). Additionally, 3T3-L1 adipocytes were treated for 24 h with T4 (100 nM) or T3 (100 nM). PAI-1 gene expression was determined by real-time PCR, while the serum concentration of PAI-1 was measured by ELISA using a commercial kit (Innovative Research, USA). Both the serum concentration of PAI-1 and mRNA levels were similar between groups in retroperitoneal and epididymal white adipose tissue. Using 3T3-L1 adipocytes, in vitro treatment with T4 and T3 increased the gene expression of PAI-1, suggesting non-genomic and genomic effects, respectively. These results demonstrate that thyroid hormones have different effects in vitro and in vivo on PAI-1 gene expression in adipocytes.

Correlation of serum leptin and insulin levels of pregnant protein-restricted rats with predictive obesity variables.

During pregnancy and protein restriction, changes in serum insulin and leptin levels, food intake and several metabolic parameters normally result in enhanced adiposity. We evaluated serum leptin and insulin levels and their correlations with some predictive obesity variables in Wistar rats (90 days), up to the 14th day of pregnancy: control non-pregnant (N = 5) and pregnant (N = 7) groups (control diet: 17% protein), and low-protein non-pregnant (N = 5) and pregnant (N = 6) groups (low-protein diet: 6%). Independent of the protein content of the diet, pregnancy increased total (F1,19 = 22.28, P < 0.001) and relative (F1,19 = 5.57, P < 0.03) food intake, the variation of weight (F1,19 = 49.79, P < 0.000) and final body weight (F1,19 = 19.52, P < 0.001), but glycemia (F1,19 = 9.02, P = 0.01) and the relative weight of gonadal adipose tissue (F1,19 = 17.11, P < 0.001) were decreased. Pregnancy (F1,19 = 18.13, P < 0.001) and low-protein diet (F1,19 = 20.35, P < 0.001) increased the absolute weight of brown adipose tissue. However, the relative weight of this tissue was increased only by protein restriction (F1,19 = 15.20, P < 0.001) and the relative lipid in carcass was decreased in low-protein groups (F1,19 = 4.34, P = 0.05). Serum insulin and leptin levels were similar among groups and did not correlate with food intake. However, there was a positive relationship between serum insulin levels and carcass fat depots in low-protein groups (r = 0.37, P < 0.05), while in pregnancy serum leptin correlated with weight of gonadal (r = 0.39, P < 0.02) and retroperitoneal (r = 0.41, P < 0.01) adipose tissues. Unexpectedly, protein restriction during 14 days of pregnancy did not alter the serum profile of adiposity signals and their effects on food intake and adiposity, probably due to the short term of exposure to low-protein diet.

Correlation of serum leptin and insulin levels of pregnant protein-restricted rats with predictive obesity variables

During pregnancy and protein restriction, changes in serum insulin and leptin levels, food intake and several metabolic parameters normally result in enhanced adiposity. We evaluated serum leptin and insulin levels and their correlations with some predictive obesity variables in Wistar rats (90 days), up to the 14th day of pregnancy: control non-pregnant (N = 5) and pregnant (N = 7) groups (control diet: 17 percent protein), and low-protein non-pregnant (N = 5) and pregnant (N = 6) groups (low-protein diet: 6 percent). Independent of the protein content of the diet, pregnancy increased total (F1,19 = 22.28, P < 0.001) and relative (F1,19 = 5.57, P < 0.03) food intake, the variation of weight (F1,19 = 49.79, P < 0.000) and final body weight (F1,19 = 19.52, P < 0.001), but glycemia (F1,19 = 9.02, P = 0.01) and the relative weight of gonadal adipose tissue (F1,19 = 17.11, P < 0.001) were decreased. Pregnancy (F1,19 = 18.13, P < 0.001) and low-protein diet (F1,19 = 20.35, P < 0.001) increased the absolute weight of brown adipose tissue. However, the relative weight of this tissue was increased only by protein restriction (F1,19 = 15.20, P < 0.001) and the relative lipid in carcass was decreased in low-protein groups (F1,19 = 4.34, P = 0.05). Serum insulin and leptin levels were similar among groups and did not correlate with food intake. However, there was a positive relationship between serum insulin levels and carcass fat depots in low-protein groups (r = 0.37, P < 0.05), while in pregnancy serum leptin correlated with weight of gonadal (r = 0.39, P < 0.02) and retroperitoneal (r = 0.41, P < 0.01) adipose tissues. Unexpectedly, protein restriction during 14 days of pregnancy did not alter the serum profile of adiposity signals and their effects on food intake and adiposity, probably due to the short term of exposure to low-protein diet.

Rice bran supplementation during nutritional recovery period of malnourished rats improves colon development.

OBJECTIVE: To investigate the colon's development in rats subjected to protein energy malnutrition followed by supplementation with rice bran. MATERIALS AND METHODS: Weaned Wistar male rats (21 days old), weight (40-50 g) were divided into two groups: diet with 17% protein (C; control group) or an aproteic diet (A; aproteic group), for 12 days. After this, 50% of the rats from each group were sacrificed. The remaining rats were further distributed in the three groups for a recovery (21 days): control (C) continued to receive the control diet whereas the aproteic group (A) received either a control diet (AC) or a control diet supplemented with 5% of rice bran (ARB). RESULTS: The A group showed alterations in the colon and cecum, excreted dry feces mass and fecal nitrogen, compared with C rats. In the proximal colon of A rats, the external muscularis and the width of the colon wall were higher whereas in the distal colon they were lower than C. After the recovery period, the relative cecum mass, colon mass and colon length of the recovered groups (AC and ARB) were higher than in the C group. Dry feces and fecal nitrogen excreted of the rats from recovered groups were lower than C group. Colon length of the AC group was lower than in the C group. Only the crypt's depth from ARB group was higher than in the C group. CONCLUSION: Control diet supplemented with 5% rice bran, reestablished the large intestine of aproteic rats. The recovery in the ARB group was even better than in the AC rats.

Lipid metabolism of monosodium glutamate obese rats after partial removal of adipose tissue.

We analyzed the effects of partial fat pad removal on retroperitoneal and epididymal fat depots and carcass metabolism of control (C) and MSG-obese (M) rats. Three-month-old C and M male Wistar rats were submitted to either partial surgical excision of epididymal and retroperitoneal fat tissue (lipectomy, L) or sham surgery (S) and studied after 7 or 30 days. Retroperitoneal and epididymal tissue re-growth after lipectomy was not observed, as indicated by the low pads weight of the L groups. The lipolysis rate was stimulated in LC7 and LM7, probably due to surgical stress and low insulin levels. In LM7, but not in LC7, in vivo lipogenesis rate increased in retroperitoneal and epididymal fat tissue, as did the diet-derived lipid accumulation in epididymal fat tissue. Although these local increases were no longer present in LM30, this group showed a large increase in the percentage of small area adipocytes in both pads as well as increased carcass lipogenesis rate. The present data showed that the partial removal of fat depots affected the metabolism of control and MSG-obese rats differently. In the obese animals only, it stimulated both local and carcass lipogenesis rate as well as adipocyte differentiation, i.e. responses likely to favor excised tissue re-growth and/or compensatory growth of non-excised depots.

Effect of ethanol intake during lactation on male and female pups' liver and brain metabolism during the suckling-weaning transition period.

In rats, a high degree of brain development and myelination occurs during the first 15 days after birth. Ethanol intake by lactating rats modified 12 day-old pups' brain development and metabolism. The aim of the present study was to evaluate the effect of maternal ethanol ingestion during lactation on prepubertal (24-day-old) pups' brain and liver metabolism. Lactating rats (4 male and 4 female litters) were divided into 2 groups: control--received control liquid diet, and ethanol--received liquid diet containing 4% of ethanol. On postnatal day 24, the pups were killed by decapitation. Liver and brain were utilized for measuring Adenosine Tri-phosphate-citrate lyase and malic enzymes activities. Brain slices were incubated in medium containing glucose to determine glucose consumption and oxidation, and lipid synthesis. The ethanol intake decreased male and female pups' body, brain and liver weight. Liver Adenosine Tri-phosphate-citrate lyase activity was decreased only in male pups of the ethanol group. The intake of ethanol solution by the dams increased glucose consumption and oxidation by the incubated female pups' brain slices and decreased glucose oxidation by the male pups' brain slices. It can be concluded that the effects of maternal ethanol intake on pups' development and metabolism are gender-related.

Ethanol intake during lactation. I. Effects On dams' metabolism and pups' body weight gain.

Wistar lactating rats (8 pups per dam) had free access to either tap water (control group, C) or one of three concentrations of ethanol (E) in the drinking water: 5% (E5), 10% (E10), and 20% (E20). All animals received normal rat chow ad libitum and were killed on day 12 of lactation. Intake of both 10% and 20% ethanol solutions decreased food intake, dams' body weight, and pups' body weight gain as compared with findings in the C group. The relative weights (g/100g b.w.) of the mammary glands (MG) and of the parametrial white adipose tissue depot were decreased only in E20 as compared with findings in the C group. Protein and lipid content of these tissues were not altered in any of the ethanol groups. In comparison with the C group, the lipogenesis rate was increased in the MG (135. 6%) and liver (120.2%) in E5 and the MG (58.1%) and parametrial white adipose tissue depot (147.0%) in E20. No modifications in lipogenesis rate were noted in E10. The malic enzyme activity was decreased in the MG in E10 (25.3%) and E20 (26.4%) and in the liver in E20 (45.7%). In E5, however, it was increased in the liver (23. 9%). The activity of ATP-citrate lyase in the liver was decreased in E20 (56.7%), while it was increased by 37.5% in E5 and 34.2% in E10. Blood glucose concentration of dams was not affected by ethanol ingestion. However, plasma triacylglycerol concentration was higher in E10 (17.9%) and E20 (13.3%) than in the C group, and plasma protein was lower in E20 (15.7%) than in C. We concluded that alcohol intake during lactation increased the MG lipogenesis rate; although at the highest dose, this metabolic alteration was not enough to allow normal pups' growth. However, the low dose of ethanol (5%), despite having altered dams' metabolism, did not affect pups' body weight gain.

Ethanol intake during lactation. II. Effects On pups' liver and brain metabolism.

Lactating rats, with litters adjusted to 8 pups on day 1, were divided into 4 groups: control animals (C), which received water and Nuvilab chow ad libitum, and ethanol animals (E), which received 20% (E20), 10% (E10), or 5% (E5) ethanol diluted in the drinking water and Nuvilab chow ad libitum. On day 12 of life, the pups were weighed and decapitated. The intake of 10% and 20% ethanol solutions by the lactating rats decreased the pups' body weight and liver weight. The pups' liver ATP-citrate lyase activity was decreased in all ethanol groups. The pups' brain weight decreased in E20 only. Glucose metabolism and lactate production were studied in the pups' brain slices, which were incubated at 37 degrees C in Krebs-Henseleit buffer under carbogen in the presence of glucose (5 mM) plus 14C-glucose (0.04 microCi) with or without beta-hydroxybutyrate or insulin. Study of the incubated pups' brain slices showed that the intake of the 20% ethanol solution by the dams increased glucose consumption, oxidation, lactate production, and lipogenesis rate from glucose in all media studied, as compared with findings in the C group. In the pups' brain slices, the lactate production and lipogenesis rate from glucose were higher in E10 than in the C group. The addition of beta-hydroxybutyrate to the incubation medium caused a decrease in glucose oxidation in C, E5, and E20 and an increase in glucose consumption in E10. Ingestion of the 5% ethanol solution by dams decreased the pups' brain lipogenesis rate from glucose in all media studied. We concluded that the effects of maternal alcohol intake on the pups' development and metabolism are dose-dependent. High amounts of ethanol intake (10% or 20%) caused a great impairment in the pups' growth, as well as their liver and brain metabolism. The low dose (5%) did not affect the pups' body weight gain or their brain and liver weight, but it did alter brain glucose metabolism.

Ethanol intake during lactation impairs milk production in rats and affects growth and metabolism of suckling pups.

From parturition, lactating Wistar rats were given 20% alcohol in drinking water and fed a solid diet ad lib (group AL). Pair-fed (PF) and control (C) rats were fed solid diet and given water ad lib (C). All animals were sacrificed on the 12th day of lactation. Ethanol treatment decreased food intake and milk production in lactating rats to a greater level than in PF rats, and a greater reduction in body weight of the AL pups was noted. Brain weight, protein concentration, and DNA content were also lower in pups of AL dams than of PF dams, whereas liver glycogen concentration was higher in the former. Pups from AL dams had higher circulating levels of beta-OH-butyrate, triglyceride, and free fatty acids than those from either C or PF dams. Plasma glucose concentration was lower in both PF and AL than in C pups, whereas the AL group had lower plasma protein concentration than any of the other groups. We conclude that maternal alcohol intake during lactation greatly impairs milk production, and although the known increase of lipid content in milk in rats studied under similar conditions allows an enhanced lipidic components in the pups, this adaptation does not allow normal growth and brain development.

Hormonal and metabolic adaptations to fasting in monosodium glutamate-obese rats.

The effect of fasting on hormonal and metabolic variables was evaluated in normal rats and in rats with obesity induced by neonatal treatment with monosodium glutamate (MSG). The hyperinsulinemia of the fed obese rats was reversed by fasting. Plasma corticosterone was also high in the fed obese and decreased to levels similar to fed controls, while it increased in the latter group during fasting. In contrast, thyroid hormone levels decreased in controls but increased in the obese rats in response to fasting. The fed obese group had lower carcass protein and higher carcass lipid contents than controls. In response to fasting, the decrements of the initial amount of both protein and fat were lower in MSG than in controls. Fasting induced a sustained increase in plasma free fatty acids only in the obese rats, although a single 100 mumol.l-1 dose of norepinephrine stimulated in vitro glycerol release more pronouncedly in epididymal adipocytes from control than obese rats. The results indicate that MSG-obese rats were able to mobilize fat stores during prolonged fasting. The high availability of lipid fuels and the sharp and sustained decrease in circulating corticosterone in the MSG group were probably important in diminishing body protein consumption during fasting.

Effects of ethanol intake on lipid metabolism in the lactating rat.

Female rats receiving alcohol (20%) in drinking water during lactation (AL) were compared to pair-fed animals (PF) and normal controls (C) fed ad lib. All animals were killed on the 12th day of lactation. When compared to C rats, food intake decreased in both AL and PF groups, and this effect was followed by a lower body weight and mammary gland (MG), liver, and parametrial adipose tissue weights. Mammary glands triacylglyceride concentration (TG) was much lower in PF than in AL, although in the latter, values did not reach those of C, and had higher liver TG concentration than any of the other groups. Both PF and AL rats had lower plasma TG, glycerol, and free fatty acid concentrations and higher beta-hydroxybutyrate concentration than C rats. When compared to C rats, the rate of lipogenesis in MG was higher in both PF and AL rats, whereas in liver it was higher in PF and lower in AL rats, and in adipose tissue it was higher in PF and unchanged in AL rats. The appearance of 14C lipids 4 h after oral [14]triolein in both MG and liver was lower in AL and PF rats and only lower in adipose tissue of AL rats as compared to the c rats. Lipoprotein lipase and hormone-sensitive lipase activities were lower in MG in both PF and AL rats than in C, whereas in adipose tissue the activity of lipoprotein lipase did not differ between AL and C rats and the activity of HSL was lower in the former. These findings therefore show that in spite of reduced uptake of orally administered triglycerides due to decreased LPL activity, maternal alcohol feeding during lactation in the rat preserves the mammary gland triglyceride content thanks to enhanced lipogenetic activity. On the other hand, it causes liver triglycerides accumulation, probably as a result of the decreased rate of triglycerides released into circulation, and these changes are not caused by the reduced food intake of the animals.

Effect of saturated and polyunsaturated fatty acids rich diets on hepatic and adipose tissue lipid metabolism in rats.

To examine the relationship between the type of dietary fat on liver and adipose tissue metabolism, in this study, fresh weight, protein, DNA, lipid content, and rate of lipogenesis from 3H2O of liver and retroperitoneal (RET) and epididymal (EPI) adipose tissues were assessed in rats fed polyunsaturated omega-6 (PUFA), saturated medium chain (SMC) or saturated long chain (SLC) fatty acid rich chows and control chow (CC). The results obtained indicate that fatty acid rich diets decreased liver fresh weight, protein and DNA content. However, they increased lipid content in liver and carcasses without changing the weight of RET and EPI. The rate of lipogenesis in vivo was increased by SMC and PUFA in liver and RET. These results indicate that not only the lipid content of diet but also the type of fatty acid caused metabolic alterations both in liver and white adipose tissues.

Re-examination of the putative roles of insulin and prolactin in the regulation of lipid deposition and lipogenesis in vivo in mammary gland and white and brown adipose tissue of lactating rats and litter-removed rats.

1. The effects of various treatments to alter either plasma prolactin (bromocryptine administration or removal of litter) or the metabolic activity of the mammary gland (unilateral or complete teat sealing) on the disposal of oral [14C]lipid between 14CO2 production and [14C]lipid accumulation in tissues of lactating rats were studied. In addition, the rates of lipogenesis in vivo were measured in mammary gland, brown and white adipose tissue and liver. 2. Bromocryptine administration lowered plasma prolactin, but did not alter [14C]lipid accumulation in mammary gland or in white and brown adipose tissue. 3. In contrast, complete sealing of teats results in no change in plasma prolactin, but a 90% decrease in [14C]lipid accumulation in mammary gland and a 4-fold increase in white and brown adipose tissue. The rate of lipogenesis in mammary gland was decreased by 95%, but there was no change in the rate in white and brown adipose tissue. Unilateral sealing of teats resulted in a decrease in [14C]lipid accumulation in white adipose tissue. 4. Removal of the litter for 24 h (low prolactin) produced a similar pattern to complete teat sealing, except that there was a 6-fold increase in lipogenesis in white adipose tissue. Re-suckling for 5 h increased plasma prolactin, but did not alter the response seen in litter-removed lactating rats. 5. Changes in lipoprotein lipase activity and in plasma insulin paralleled the reciprocal changes in [14C]lipid accumulation in white and brown adipose tissue and in mammary gland. 6. It is concluded that the plasma insulin is more important than prolactin in regulating lipid deposition in adipose tissue during lactation, and that any effects of prolactin must be indirect.